Re: Hyperthyroid advice needed

[Guest guest]

Hello ,

My husband just had some blood test results yesterday as follows:TSH <0.01 (ref 0.35-3.5)Free T4 35 (ref range 8-21)Free T3 19.2 (ref range 3.8-6.0)Clearly this indicates hyperthyroidism but I have a few concerns.

Yes, you are correct.

He was diagnosed with 's last year and in Dr Peatfield's book he says that adrenal insufficiency "makes a nonsense" of thyroid test results, but is this just when it's untreated?

First of all – was your husband diagnosed with primary or secondary 's, and what medication (and dosage) is he taking for it ? This is extremely important to know.... since you are not mentioning anything about his medication I am beginning to wonder.....

Both primary and secondary 's are very serious autoimmune diseases – primary AD is when the adrenal glands are damaged to the point where they can't produce any more mineral and glucocorticoids. Secondary AD means malfunctioning of the pituitary gland due to either a benign tumour or an adrenal tumour or brain injury etc.... Either condition would need immediate medication with either Florinef (primary AD) or HC (secondary AD).

He also had high sodium and chloride in the past, which is supposed to be low in s, and normal potassium. Sodium andpotaassium were normal last week but chloride was still high, but only just outside range.

This makes me wonder even more about the accuracy of a diagnosis for 's... at least one for primary ' – although it does depend on the correct medication. A well adjusted treatment plan with Florinef for primary 's would indeed keep the electrolytes on an even keel.... However - having said that, with secondary AD the electrolyte figures would be unaffected. Could you please tell me the actual figures for both, his ACTH simulation test (short synacthen test) and the electrolyte test? From the results of the SST and the electrolytes I could probably work things out.

Last June his TSH was 0.59 (ref 0.4-4.0), Free T4 was 15.8 (ref 10-22) and FreeT3 was 4.05 (ref 2.8-6.5) so besides the TSH being lowish, the rest was okay. In Oct 09 his TSH was 1.21.Also, the endo didn't test for antibodies but when we tested privately last June his Peroxidase were at 99. At that time I thought he might have Hashi's as he had low temps. His temps are still low and he doesn't feel `hyper', moreexhaustion and `hypo' but does have a high pulse, weight loss and muscleweakness/loss. Is it possible he's on the `hyper' swing of Hashi's?

Might be – but without knowing what is really going on it is very difficult to comment. 's and thyroid malfunction nearly always go hand in hand and it is extremely difficult to stabilize primary 's without first of all stabilizing the thyroid condition. The autoantibodies might also play havoc, and without knowing all the figures and all the medication it would be a guessing game to work out what's going on.

Other finding were low testosterone last June. I am wondering about pituitarydisease/tumour since cortisol, TSH and testosterone are all very low? I'veasked the GP to test FSH and LH, Peroxidase, Prolactin and DHEA to rule this out which will be done on Monday.

If your husband had secondary AD, this would be in most cases down to a pituitary tumour - but surely, with a serious diagnosis like 's all of this must have already been cleared up and should have been explained to your husband ???? ly, I am very confused. With all those questions open, how on earth did the doctors make a diagnosis of ? It just does not make sense.

Other test results were high Urea at 7.4 (ref 1.7-7.1), low Total Protein at 57(ref 63-82), low Albumin at 31 (ref 35-50), normal Globulin although it's alwaysbeen low in past tests, Ferritin, B12 and Folate all normal. Only otherabnormal results were high Monocytes at 1.5 (ref 0.20-0.80) and high Eosinophils at 0.47 (ref 0.04 – 0.4) – he is very allergic and eosinophils are often raised.Short synacthen test (second one done) confirmed extremely low cortisol levels.

Please do give us the figures from the SST. An SST is not just about confirming low cortisol figures, but about the possibility (or impossibility) to stimulate the adrenal glands into producing cortisol – and this - in conjunction with a serum ACTH test - would determine which kind of 's he is suffering from . I really need to see all the figures (and ref ranges) and it is very important to know if a doctor has definitely made a diagnosis of 's – or has it been called `adrenal insufficiency'? – which is a diagnosis given sometimes when the levels of cortisol are very low, but which is not caused by damaged adrenals but by severe adrenal exhaustion...there is a huge difference. - And what kind of treatment is your husband on for his 's?

Otherwise my question is – should he start on Carbimazole right away as he feels awful, or should he wait for the other blood tests to confirm whether or not it's a pituitary disease or DHEA deficiency? The GP didn't have any idea and he's not due to see the Endo for another two weeks. Is it dangerous not to treat it right away? If he starts taking it now can he just stop or does itneed to be tapered?Thanks for any advice

None of us could advise on treatment, particularly with all those question marks hanging over the diagnoses and not knowing what medication your husband is already taking. But one thing is for certain – the appointment with an endo cannot wait 2 more weeks. Due or not due, call them as soon as you can and make an emergency appointment. Unfortunately it is a weekend, but if your GP can't make a decision (and quite rightly he should not in this case if he does not fully understand any of the conditions), then the endo appointment will have to be brought forward- preferably to Monday morning. Or, if your husband is in a really bad way, then please ask at your local A & E if there is an endocrinologist on duty by any chance who could be consulted. In a bigger hospital there might be a good chance of that.

With best wishes,

[Guest guest]

Hi

Thank you so much for responding.

He has been diagnosed with primary 's he thinks, although the endo was

quite frankly useless. He's seeing a different one now who repeated the SST but

he hasn't had the appt with him yet and didn't call about his latest test

results - it was his GP who was copied in who noticed the hyperthyroidism and

called on Thursday night. Initially he took about 25 mg HC for a couple of

months but it wasn't really controlling his asthma/allergies so he went back

onto prednisolone which averages about 7 mg per day although occasionally he has

to take up to 30 mg for more acute episodes. I worry that no one seems to have

done any tests for pituitary so wonder if it is primary or secondary. I think

it's been terribly bad managed - he was on high dose steroids for asthma for

years, now has cataracts and the second endo wonders if his 's is a

result of steroid use, so possibly secondary? He said no one has ever mentioned

Florinef to him, only HC.

Sodium results:

Apr 08 143 (ref 135-145)

May 11 146 (ref 135-145)

Mar 12 142 (ref 134-145)

Chloride results:

April 08 106 (ref 98-107)

May 11 110 (ref 98-107)

Mar 12 108 (ref 98-107)

Potassium results:

Apr 08 4.6 (ref 3.5-5.1)

May 11 4.3 (ref 3.5-5.1)

Mar 12 3.9 (ref 3.6-5.0)

SST Apr 11

Basal 34 nmol/L

30 mins 107 nmol/L

60 mins 145 nmol/L

SST Mar 12

Basal 8 nmol/L

30 mins 61 nmol/L

60 mins 68 nmol/L

30 min Cortisol should be about 550 nmol/L

The last endo only wrote a letter (didn't give paper copies of test results

despite repeated requests and formal complaint) but said the thyroid was

functioning normally, this was in Apr 11.

The ACTH test has been done but results are not back yet, as well as anti

adrenal antibody, although this was negative last April.

Does this help at all or do you need the ACTH results before knowing? He's

really fed up with not knowing what's wrong with him, and no one seeming to take

any responsibility.

Any help would be really appreciated.

>

>

>

>

> Hello ,

>

> My husband just had some blood test results yesterday as follows:

>

> TSH <0.01 (ref 0.35-3.5)

> Free T4 35 (ref range 8-21)

> Free T3 19.2 (ref range 3.8-6.0)

>

> Clearly this indicates hyperthyroidism but I have a few concerns.

>

> Yes, you are correct.

>

> He was diagnosed with 's last year and in Dr Peatfield's book he

> says that adrenal insufficiency " makes a nonsense " of thyroid test

> results, but is this just when it's untreated?

>

> First of all – was your husband diagnosed with primary or secondary

> 's, and what medication (and dosage) is he taking for it ?

> This is extremely important to know.... since you are not mentioning

> anything about his medication I am beginning to wonder.....

>

[Guest guest]

--- In thyroid treatment , "cath331144" <canadacath@...> > SST Apr 11> Basal 34 nmol/L> 30 mins 107 nmol/L> 60 mins 145 nmol/L> I-> SST Mar 12> Basal 8 nmol/L> 30 mins 61 nmol/L> 60 mins 68 nmol/L> 30 min Cortisol should be about 550 nmol/L> Does this help at all or do you need the ACTH results before knowing? He's really fed up with not knowing what's wrong with him, and no one seeming to take any responsibility.Hello ,Yes, thank you, this helped a great deal. I will reply properly tomorrow as right now I am sitting in bed, typing on my iPad, which is a bit fiddly and I don't have all the references at hand.According to those SST results it is secondary s (pituitary malfunction) that your husband suffers from. I will send you all the links that will explain the interpretation tomorrow, but in a nutshell... Pathologically low cortisol baseline levels that show a doubling, tripling or a multiple rise of the baseline cortisol level after 60 minutes is diagnostic for secondary s. However - had your husband been on any kind of steroids before the first SST in April 11? If yes, then I am not sure how accurate the test result had been. He obviously had been on steroids for the second test in March 12, and I would imagine that the result is so dramatic because of that( from 8 to 68 in one hour), but even if your husband had been on steroids when the first test was done, I am pretty sure that the diagnosis of secondary AD is correct as the baseline level tripled. They should have done (but probably hadnt) a serum ACTH test at the same time, which would have been low and that would have confirmed the diagnosis.Secondary AD is in most cases caused by a benign tumour on the pituitary gland (but can have other causes) and your husband needs further tests like an MRI scan to determine the position of a possible adenoma (benign growth) to see if this growth ( if this is what is causing the AD) can be surgically removed. If it were possible to get to it and remove it, a cure would be possible. If surgery were not an option, then the treatment is HC or Prednisolone, usually HC. Florinef would not be needed at this point, because the adrenals are not damaged and still produce Aldosterone to regulate the electrolytes; the fault is with the pituitary. I'll explain it all a bit better tomorrow. If you were living not too far from London, I could recommend an endocrinologist at King's hospital to you, who specialises in the more complicated cases. If there were a tumour and surgery were possible, you would need a very experienced surgeon. He does NHS, but it might be a longish wait. Private treatment would probably be out of the question as this guy is hellishly expensive - unless you had private insurance. more tomorrow...With best wishes,

[Guest guest]

Hello ,

Right.... here is the rest of the information –

No doubt there will be endless info from various sources on the net, but it is always best to stick to "official" references, as that is what the doctors will do too.

http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/adrenal_disorders/secondary_adrenal_insufficiency.html

It basically repeats what I told you yesterday, only in a more scientific language. It also answers your question –

....he was on high dose steroids for asthma for years, now has cataracts and the second endo wonders if his 's is aresult of steroid use, so possibly secondary?

Secondary adrenal insufficiency may occur in panhypopituitarism, in isolated failure of ACTH production, in patients receiving corticosteroids, or after corticosteroids are stopped. Inadequate ACTH can also result from failure of the hypothalamus to stimulate pituitary ACTH production, which is sometimes called tertiary adrenal insufficiency.

So yes, high steroid use over a long period is quite a possible cause for secondary 's, but IMHO an MRI scan (preferably with contrast dye, as tumours can be tiny and difficult to spot) should still be performed to rule out that possibility rather than to make assumptions. As you can read above, tertiary adrenal insufficiency should also be considered. You have a right to know what you are dealing with to consider all the treatment options.

Since you have read Dr. Peatfield's book (in Chapter two, "How it Works"), you will no doubt be familiar with the chain of events in our bodies, but let me briefly outline - telegram style - which gland does what.

The hypothalamus (half brain, half gland) receives all the information from inside and outside the body and gives signals to the pituitary. The pituitary produces many `trophic' hormones which are passed to other endocrine glands and tissues; among those there is TSH and ACTH. TSH goes to the thyroid gland to order thyroid hormone, ACTH goes to the adrenals and the amount of ACTH determines how much cortisol the adrenals have to produce. When the hypothalamus or pituitary malfunction (for whatever reason) the amount of ACTH is either too high (which leads to Cushing's), or, as in your husband's case, too low. In theory his adrenals could produce whatever is required, but they will only produce what is asked for (by the amount of ACTH)... without sufficient cortisol we cannot live, and our thyroid cannot work normally. I do not know much about tertiary 's (failure of hypothalamus), but if the pituitary is at fault, then the treatment options (I know of) are either removing the growth that causes the malfunction (if that were possible – it is not always... due to location of the tumour) or (with other causes for the malfunction or the inaccessibility to a tumour) you have to replace the amount of glucocorticoid that the adrenal glands will not produce... which means life-long supplementation with either HC or Prednisolone.

Having said that... in most (but not all) cases secondary 's can in the fullness of time (many years) turn into primary 's. This happens because the adrenal glands will eventually stop the function of their outer layer, which is the production of mineralcorticoids, mainly aldosterone. Aldosterone regulates the fluid and electrolyte balance. It retains sodium and balances the loss of potassium in the bloodstream. As you probably know, a serious imbalance of the electrolytes can be extremely dangerous. In primary 's , due to the lack of aldosterone, the sodium will fall through the floor, and the potassium will rise to dangerously high levels and the result of that would be acute kidney and heart failure. At present your husband's electrolyte are fine, so the outer cortex of his adrenals seem to be working. However, I would instigate regular electrolyte blood checks (GP can do this), particularly at times when your husband feels decidedly unwell. Better to be safe than sorry. – Just for interest, below is the info on primary 's – please note the "typical" blood test results that usually present with primary AD, so you know which tests to ask for in regular intervals and you can follow the progress. http://www.merckmanuals.com/professional/endocrine_and_metabolic_disorders/adrenal_disorders/addisons_disease.html

As for whether to best use HC or Prednisolone or which dosages, your endo will have to advise on that. The dosages of 7 mg preds (and upping whenever necessary) on average sound about right to me. Dr. P. states in his book that a body needs between 40 – 60 mg of HC per day in a normal resting state (but as much as 200 mg under stress) .... 7 mg pred equates to 35 mg of HC, and his own adrenals can be expected to still add a little cortisol to that, so 7 – 10 mg preds per day should be about right.

Re the thyroid function.... I know that in all cases of 's (primary and secondary) the thyroid function is affected, usually hypothyroidism. I have not heard of hyperthyroidism going with it, but that does not mean it can't be. - Not because of the new SST results, but because of the thyroid results I would make an emergency appointment for tomorrow with the endo, if at all possible. Since you said a blood test is due tomorrow anyway, please make sure they check for TPO, TgAB and TSI .... TSI are the antibodies against Graves disease (Hyperthyroidism). If those thyroid figures of your husband's are true and not some erroneous Hashi elevation, then he would have TSI autoantibodies. If he does not have TSI autoantibodies then to my mind (although I am not an expert on this) the elevated FT's might be a red herring. Dr. Peatfield's advice is – quote – The first approach is an alert and informed assessment of progress, intervening only when necessary. Over-intervention is the curse of modern medicine in almost any illness you can imagine; we should take to heart that sometimes a policy of `masterly inactivity' is much better for the patient and may even spare his life. – unquote –

Endo's, to my mind, are almost always too gung-ho with the use of Carbimazole. I am not familiar with dosages, but I know from a friend that a softly, softly approach – if Carbimazole were necessary at all – is the better one.... so a low dosage, which might be a fraction of what the endos recommend, is usually better to prevent "overshooting". I am sure some of our Graves members will be able to tell you about their experiences.

This is all I can think of for now – if you have any questions, just shout.

Best of luck for your husband and with warm wishes,

PS - I will pm you the name of the endo in London in a minute, just in case London were a possibility for you.

[Guest guest]

Hi , Dr P is correct. the low adrenals will affect the tests for thyroid

function. the TSH and other tests will change somewhat if an attack of

auto-antibodies are at work. you can have thyroid auto.antibodies in hashimoto`s

and graves disease.!!! angel.

>

> Hi

>

> My husband just had some blood test results yesterday as follows:

>

> TSH <0.01 (ref 0.35-3.5)

> Free T4 35 (ref range 8-21)

> Free T3 19.2 (ref range 3.8-6.0)

>

> Clearly this indicates hyperthyroidism but I have a few concerns. He was

diagnosed with 's last year and in Dr Peatfield's book he says that

adrenal insufficiency " makes a nonsense " of thyroid test results, but is this

just when it's untreated? He also had high sodium and chloride in the past,

which is supposed to be low in s, and normal potassium. Sodium and

potaassium were normal last week but chloride was still high, but only just

outside range.

>

> Last June his TSH was 0.59 (ref 0.4-4.0), Free T4 was 15.8 (ref 10-22) and

Free T3 was 4.05 (ref 2.8-6.5) so besides the TSH being lowish, the rest was

okay. In Oct 09 his TSH was 1.21.

>

> Also, the endo didn't test for antibodies but when we tested privately last

June his Peroxidase were at 99. At that time I thought he might have Hashi's as

he had low temps. His temps are still low and he doesn't feel `hyper', more

exhaustion and `hypo' but does have a high pulse, weight loss and muscle

weakness/loss. Is it possible he's on the `hyper' swing of Hashi's?

>

> Other finding were low testosterone last June. I am wondering about pituitary

disease/tumour since cortisol, TSH and testosterone are all very low? I've

asked the GP to test FSH and LH, Peroxidase, Prolactin and DHEA to rule this out

which will be done on Monday.

>

> Other test results were high Urea at 7.4 (ref 1.7-7.1), low Total Protein at

57 (ref 63-82), low Albumin at 31 (ref 35-50), normal Globulin although it's

always been low in past tests, Ferritin, B12 and Folate all normal. Only other

abnormal results were high Monocytes at 1.5 (ref 0.20-0.80) and high Eosinophils

at 0.47 (ref 0.04 – 0.4) – he is very allergic and eosinophils are often raised.

> Short synacthen test (second one done) confirmed extremely low cortisol

levels.

>

> If anyone has any other insight into these test results I would appreciate it.

>

> Otherwise my question is – should he start on Carbimazole right away as he

feels awful, or should he wait for the other blood tests to confirm whether or

not it's a pituitary disease or DHEA deficiency? The GP didn't have any idea

and he's not due to see the Endo for another two weeks. Is it dangerous not to

treat it right away? If he starts taking it now can he just stop or does it

need to be tapered?

> Thanks for any advice

>

>